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NEPHROLOGY / BASIC RESEARCH
Important role of long non-coding RNA UBE2R2-AS1 in diabetes-induced renal injury
1
Endocrinology Department, Shekou People’s Hospital, Nanshan District, Shenzhen, Guangdong, China
Submission date: 2020-01-26
Final revision date: 2020-02-26
Acceptance date: 2020-03-07
Online publication date: 2020-11-06
Publication date: 2025-04-23
Corresponding author
Chuanqi Chen
Endocrinology Department, Shekou People’s Hospital, Nanshan District, Shenzhen, Guangdong, China
Endocrinology Department, Shekou People’s Hospital, Nanshan District, Shenzhen, Guangdong, China
Arch Med Sci 2025;21(2):617-629
KEYWORDS
TOPICS
ABSTRACT
Introduction:
The present study examined the effects and mechanisms underlying long non-coding RNA (lncRNA) UBE2R2-AS1 in diabetes-induced renal injury.
Material and methods:
High glucose was used to imitate diabetes-induced renal injury in a cell model. Cell apoptosis rate was measured using flow cytometry, tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6) concentrations were evaluated using ELISA, and relative protein expression and amount were measured using western blot (WB) analysis and immunofluorescence, respectively. Correlations between lncRNA UBE2R2-AS1, miRNA-877-3p and TLR4 were analysed using the luciferase reporter assay.
Results:
Cell apoptosis rate and TNF-a and IL-6 concentrations were significantly higher (p < 0.001) in the high glucose (model) group compared with those of the Control group (CG) group. Following shRNA knockdown of lncRNA UBE2R2-AS1, the cell apoptosis rate and TNF-a and IL-6 concentrations were significantly lower (p < 0.001, respectively) compared with those of the model group. However, under high-glucose conditions, shRNA knockdown of UBE2R2-AS1 and miRNA-877-3p significantly increased (p < 0.001) the cell apoptosis rate as well as TNF-a and IL-6 concentrations compared with the shRNA UBE2R2-AS1 knockdown group. WB and immunofluorescence analysis showed that toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor κB (p65) (NF-κB(p65)) pathway proteins were significantly stimulated in the model group compared with those in the CG, whereas shRNA transfection with miRNA-877-3p stimulation suppressed the TLR4/MyD88/NF-B(p65) pathway.
Conclusions:
Knockdown of lncRNA UBE2R2-AS1 improves diabetes-induced renal injury via regulation of the miRNA-877-3p/TLR4 axis in vitro.
The present study examined the effects and mechanisms underlying long non-coding RNA (lncRNA) UBE2R2-AS1 in diabetes-induced renal injury.
Material and methods:
High glucose was used to imitate diabetes-induced renal injury in a cell model. Cell apoptosis rate was measured using flow cytometry, tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6) concentrations were evaluated using ELISA, and relative protein expression and amount were measured using western blot (WB) analysis and immunofluorescence, respectively. Correlations between lncRNA UBE2R2-AS1, miRNA-877-3p and TLR4 were analysed using the luciferase reporter assay.
Results:
Cell apoptosis rate and TNF-a and IL-6 concentrations were significantly higher (p < 0.001) in the high glucose (model) group compared with those of the Control group (CG) group. Following shRNA knockdown of lncRNA UBE2R2-AS1, the cell apoptosis rate and TNF-a and IL-6 concentrations were significantly lower (p < 0.001, respectively) compared with those of the model group. However, under high-glucose conditions, shRNA knockdown of UBE2R2-AS1 and miRNA-877-3p significantly increased (p < 0.001) the cell apoptosis rate as well as TNF-a and IL-6 concentrations compared with the shRNA UBE2R2-AS1 knockdown group. WB and immunofluorescence analysis showed that toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor κB (p65) (NF-κB(p65)) pathway proteins were significantly stimulated in the model group compared with those in the CG, whereas shRNA transfection with miRNA-877-3p stimulation suppressed the TLR4/MyD88/NF-B(p65) pathway.
Conclusions:
Knockdown of lncRNA UBE2R2-AS1 improves diabetes-induced renal injury via regulation of the miRNA-877-3p/TLR4 axis in vitro.
REFERENCES (29)
2.
Yu R, Zhang Y, Lu Z, et al. Long-chain non-coding RNA UCA1 inhibits renal tubular epithelial cell apoptosis by targeting microRNA-206 in diabetic nephropathy. Arch Physiol Biochem 2019; 12: 1-9.
3.
Kato M, Wang M, Chen Z, et al. An endoplasmic reticulum stress regulated lncRNA hosting a microRNA megacluster induces early features of diabetic nephropathy. Nat Commun 2016; 7: 12864.
4.
Kaczmarczyk-Sedlak I, Folwarczna J, Sedlak L, et al. Effect of caffeine on biomarkers of oxidative stress in lenses of rats with streptozotocin-induced diabetes. Arch Med Sci 2019; 15: 1073-80.
5.
Guo J, Liu Z, Gong R. Long noncoding RNA: an emerging player in diabetes and diabetic kidney disease. Clin Sci 2019; 133: 1321-39.
6.
Santer L, López B, Ravassa S, et al. Circulating long noncoding RNA LIPCAR predicts heart failure outcomes in patients without chronic kidney disease. Hypertension 2019; 73: 820-8.
7.
Wang M, Wang S, Yao D, et al. A novel long non-coding RNA CYP4B1-PS1-001 regulates proliferation and fibrosis in diabetic nephropathy. Mol Cell Endocrinol 2016; 426: 136-45.
8.
Klisic A, Kavaric N, Stanisic V, et al. Endocan and a novel score for dyslipidemia, oxidative stress and inflammation (DOI score) are independently correlated with glycated hemoglobin (HbA1c) in patients with prediabetes and type 2 diabetes. Arch Med Sci 2019; 16: 42-50.
9.
Zhu L, Zhao S, Liu S, et al. PTEN regulates renal extracellular matrix deposit via increased CTGF in diabetes mellitus. J Cell Biochem 2016; 117: 1187-98.
10.
McClelland AD, Herman-Edelstein M, Komers R, et al. miR-21 promotes renal fibrosis in diabetic nephropathy by targeting PTEN and SMAD7. Clin Sci 2015; 129: 1237-49.
11.
Zhou M, Zhang Z, Zhao H, et al. An immune-related six-lncRNA signature to improve prognosis prediction of glioblastoma multiforme. Mol Neurobiol 2018; 55: 3684-97.
12.
Xu W, Hu GQ, Da Costa C, et al. Long noncoding RNA UBE2R2-AS1 promotes glioma cell apoptosis via targeting the miR-877-3p/TLR4 axis. Onco Targets Ther 2019; 12: 3467-80.
13.
Verhoeven RJA, Tong S, Mok BW, et al. Epstein-Barr virus BART long non-coding RNAs function as epigenetic modulators in nasopharyngeal carcinoma. Front Oncol 2019; 9: 1120.
14.
Luo J, Qu J, Wu DK, et al. Long non-coding RNAs: a rising biotarget in colorectal cancer. Oncotarget 2017; 8: 22187-202.
15.
Dey N, Bera A, Das F, et al. High glucose enhances microRNA-26a to activate mTORC1 for mesangial cell hypertrophy and matrix protein expression. Cell Signal 2015; 27: 1276-85.
16.
Zhou L, Xu DY, Sha WG, Shen L, Lu GY, Yin X. Long non-coding MIAT mediates high glucose-induced renal tubular epithelial injury. Biochem Biophys Res Commun 2015; 468: 726-32.
17.
Yan B, Yao J, Liu JY, et al. lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA. Circ Res 2015; 116: 1143-56.
18.
Liao J, He Q, Li M, et al. LncRNA MIAT: Myocardial infarction associated and more. Gene 2016; 578: 158-61.
19.
Li Z, Shen J, Chan MT, et al. TUG1: a pivotal onvogeic long non-coding RAN of human cancers. Cell Prolif 2016; 49: 471-5.
20.
Li J, Zhang M, An G, et al. LncRNA TUG1 acts as a tumor suppressor in human glioma by promoting cell apoptosis. Exp Biol Med 2016; 241: 644-9.
21.
Gong DJ, Wang L, Yang YY, et al. Diabetes aggravates renal ischemia and reperfusion injury in rats by exacerbating oxidative stress, inflammation, and apoptosis. Ren Fail 2019; 41: 750-61.
22.
Zhu L, Han J, Yuan R, et al. Berberine ameliorates diabetic nephropathy by inhibiting TLR4/NF-kappaB pathway. Biol Res 2018; 51: 9.
23.
Su S, Zhang P, Zhang Q, Yin Z. GSK-3beta Inhibitor Induces expression of the TLR4/MyD88/NF-kappaB signaling pathway to protect against renal ischemia-reperfusion injury during rat kidney transplantation. Inflammation 2019; 42: 2105-18.
24.
Lei J, Fu Y, Zhuang Y, et al. miR-382-3p suppressed IL-1beta induced inflammatory response of chondrocytes via the TLR4/MyD88/NF-kappaB signaling pathway by directly targeting CX43. J Cell Physiol 2019; 234: 23160-8.
25.
Ibrahim YF, Moussa RA, Bayoumi AMA, et al. Tocilizumab attenuates acute lung and kidney injuries and improves survival in a rat model of sepsis via down-regulation of NF-kappaB/JNK: a possible role of P-glycoprotein. Inflammopharmacology 2020; 28: 215-30.
26.
Yang ZJ, Wang HR, Wang YI, et al. Myricetin attenuated diabetes-associated kidney injuries and dysfunction via regulating nuclear factor (erythroid derived 2)-like 2 and nuclear factor-kappaB signaling. Front Pharmacol 2019; 10: 647.
27.
Ma F, Li L, Wang Q, et al. Qi-dan-di-huang decoction alleviates diabetic nephropathy by inhibiting the NF-kappaB pathway. Front Biosci 2019; 24: 1477-86.
28.
Duan LJ, Ding M, Hou LJ, et al. Long noncoding RNA TUG1 alleviates extracellular matrix accumulation via mediating microRNA-377 targeting of PPARgamma in diabetic nephropathy. Biochem Biophys Res Commun 2017; 484: 598-604.
29.
Li X, Zeng L, Cao C, et al. Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy. Exp Cell Res 2017; 350: 327-35.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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